The audiogenic seizure-shock episode of Mg deficiency was studied in weanling rats, with emphasis on pulmonary pathology and on means of aborting the syndrome. Lungs studied in Mg-deficient weanling rats that were killed immediately after shock revealed pathology compatible with many forms of shock, including the respiratory distress syndrome of the human infant. These included denuded basement membranes of the alveoli, and components of the basement membrane (fibrin, precipitated plasma protein, erythrocytes, and cellular debris) within the alveoli. The lungs were edematous, showed hemorrhage and atelectasis, and were essentially airless. Lung of Mg-deficient rats that were undisturbed after the seizure-shock revealed pathology compatible with that of the sudden infant death syndrome (SIDS). After the acute attack, 28 g animals silently and quickly died, while 35-40 rats experienced hyperventilation and hyperextension of the limbs and cervical spine that served to expand the lungs. Their lungs were will inflated, showed pleural petechiae, with areas of congestion, atelectasis and only mild to moderate edema with occasional hemorrhage. Most of the alveolar spaces clean; the pathology was insufficient to explain death. Studied to abort the audiogenic seizure-shock episode of Mg- deficient weanling rats showed that Mg in high doses resulting in unacceptably high plasma Mg values did not protect from seizure activity. Methylprednisolone in high doses did not fully protect from seizures. The combination of reduced Mg dosage and high methylprednisolone given 15-20 min before auditory stress did protect from seizures. Ibuprofen gave full protection from seizures under similar experimental conditions. A Squibb thromboxane A2 receptor blocker given 15-20 min before challenge modified the episode and aborted tetany, but did not fully protect; it apparently works with other mediators of shock in the pathogenesis of the episode. This is under study.